YABBY and diverged KNOX1 genes shape nodes and internodes in the stem

Katsutoshi Tsuda*, Akiteru Maeno, Ayako Otake, Kae Kato, Wakana Tanaka, Ken-Ichiro Hibara, and Ken-Ichi Nonomura
* Corresponding author

Science (2024) 384, 1241-1247 DOI:10.1126/science.adn6748

Press release (In Japanese only)

Plant stems comprise nodes and internodes that specialize in solute exchange and elongation. However, their boundaries are not well defined, and how these basic units arise remains elusive. In rice with clear nodes and internodes, we found that one subclade of class I knotted1-like homeobox (KNOX1) genes for shoot meristem indeterminacy restricts node differentiation and allows internode formation by repressing YABBY genes for leaf development and genes from another node-specific KNOX1 subclade. YABBYs promote nodal vascular differentiation and limit stem elongation. YABBY and node-specific KNOX1 genes specify the pulvinus, which further elaborates the nodal structure for gravitropism. Notably, this KNOX1 subclade organization is specific to seed plants. We propose that nodes and internodes are distinct domains specified by YABBY–KNOX1 cross-regulation that diverged in early seed plants.

Source: Katsutoshi Tsuda et al., Science (2024) 384, 1241-1247

Kawakami Group / Laboratory of Molecular and Developmental Biology

A novel gene‐trap line reveals the dynamic patterns and essential roles of cysteine and glycine‐rich protein 3 in zebrafish heart development and regeneration.

Shuzhang Liang, Yating Zhou, Yue Chang, Jiayi Li, Min Zhang, Peng Gao, Qi Li, Hong Yu, Koichi Kawakami, Jinmin Ma, and Ruilin Zhang.

Cellular and Molecular Life Sciences (2024) 81, 158 DOI:10.1007/s00018-024-05189-

CSRP3/MLP, a key regulator of striated muscle function, have been linked to hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) in patients. However, the roles of CSRP3 in heart development and regeneration are not completely understood. In this study, we characterized a novel zebrafish gene-trap line, gSAIzGFFM218A, which harbors an insertion in the csrp3 genomic locus. We discovered that csrp3 is specifically expressed in larval ventricular cardiomyocytes (CMs) and that csrp3 deficiency leads to excessive trabeculation, a common feature of CSRP3-related HCM and DCM. We further revealed that csrp3 expression increased in response to different cardiac injuries and was regulated by several signaling pathways vital for heart regeneration. Csrp3 deficiency impeded heart regeneration by impairing CM dedifferentiation, hindering sarcomere reassembly, and reducing CM proliferation while aggravating apoptosis. Csrp3 overexpression promoted CM proliferation after injury and ameliorated the impairment of ventricle regeneration caused by pharmacological inhibition of multiple signaling pathways. Our study highlights the critical role of Csrp3 in both heart development and regeneration, and provides a valuable animal model for further functional exploration that will shed light on the molecular pathogenesis of CSRP3-related human cardiac diseases.

This study was conducted as a collaborative research between the Zhang Lab at Wuhan University and the Kawakami Laboratory.　This study was supported by NIG-JOINT (2015 Collaborative Research A1-8).

Figure: Induction of csrp3 gene expression in the atrium of the heart after ventricular cardiomyocyte ablation
(Red) Expression of mCherry-NTR in the ventricular cardiomyocytes. Cells were ablated by addition of MTZ.
(Green) Induction of csrp3 gene expression in the heart after ventricular cardiomyocyte ablation.